ObjectivesOur group previously found that LINC00665 was upregulated in hepatocellular carcinoma (HCC) tissues through database analysis; however, the potential molecular mechanism of LINC00665 in HCC progression still needs further study.MethodsqRTPCR was performed to determine the differential expression of LINC00665 and let-7i in HCC cells. Dual-luciferase reporter assays were performed to analyze the interaction of LINC00665 and let-7i. CCK-8 assays, scratch assays, Transwell invasion assays, qRTPCR and western blotting were performed to determine the regulatory mechanism of LINC00665/let-7i/HMGA1 in HCC cells.ResultsLINC00665 was upregulated in HCC cells compared with normal hepatocytes. A potential binding site between LINC00665 and let-7i was confirmed by dual-luciferase reporter assay. In HCC cells, inhibition of LINC00665 significantly reduced cell proliferation, migration and invasion ability via the let-7i/HMGA1 signaling axis.ConclusionLINC00665 promotes the proliferation and invasion of HCC cells via the let-7i/HMGA1 signaling axis.

MiR-519e-5p and CTPS1 are aberrantly expressed in breast cancer (BC). However, the molecular mechanisms underlying tumorigenesis and development are unknown, and their potential as therapeutic targets needs to be explored. The molecular biology was explored through in vitro cellular experiments, tumor xenograft assay, and analysis of gene expression in human tissue and serum samples. We found that miR-519e-5p expression was much lower and CTPS1 expression was much higher in BC tissues and cells than in the normal tissues and cells. BC cells overexpressing miR-519e-5p or CTPS1 knockdown demonstrated decreased proliferation, migration, and invasion, whereas miR-519e-5p knockdown had the opposite effect. Further studies showed that there is a binding site between miR-519e-5p and CTPS1, leading to their interaction, CTPS1 overexpression and could partially reverse the inhibitory effects of miR-519e-5p overexpression on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). CTPS1 serum levels were higher in patients with BC, and these levels were associated with some highly correlated clinical indicators, including age, HER-2 index, and T and N staging. Overall, miR-519e-5p slows the proliferation, invasion, migration, and EMT of BC by binding to CTPS1. This study offers a new direction for BC treatment.

Background: Among primary liver cancers, HCC is the most prevalent. Small noncoding RNAs called miRNAs control the expression of downstream target genes to take part in a variety of physiological and pathological processes, including those related to cancer. Methods: miR-129-2-3p and SEMA4C expression levels were assessed using RT-qPCR. The CCK-8, invasion, and wound healing assays were used to confirm the capacity of HCC cells for proliferation, invasion and migration respectively. Serum SEMA4C levels were detected via ELISA. The RIP and dual-luciferase reporter assays were used to confirm the existence of intergenic binding sites. Cell apoptosis assay and cell cycle assay were performed to detect the apoptosis rate and cycle distribution of cells, and WB was performed to detect the protein expression of SEMA4C, RhoA, ROCK1, E-cadherin, N-cadherin, and vimentin. Furthermore, cancer-inhibiting role of miR129-2-3p were further confirmed by animal tests. Results: miR-129-2-3p expression was reduced in HCC tissues and cells. Overexpression of miR-129-2-3p decreased the proliferation, invasion, migration, and EMT in HCC cells, whereas inhibition of miR-129-2-3p had the opposite effects. Our research also showed that SEMA4C was increased in HCC tissues, serum and cells, and that SEMA4C knockdown prevented HCC cell invasion, migration, proliferation, and EMT. Overexpression of SEMA4C reversed the inhibitory effect of miR-129-2-3p on HCC. Conclusions: Overall, we discovered that through binding to SEMA4C, miR-129-2-3p regulates HCC cell proliferation, invasion, migration, and EMT.

目的 探讨环状RNA(hsa_circ_0000741)对乳腺癌癌细胞增殖、迁移和侵袭的影响及分子机制.方法 通过R语言limma包分析GSE182471 和GSE165884 数据集;通过常规培养乳腺癌细胞系MCF-7、MDA-MB-231 和正常细胞系MCF-10A,提取细胞总RNA,逆转录后进行qRT-PCR测定目的基因表达量;通过lipo2000 转染si-hsa_circ_0000741 对目的基因进行敲减,将其编为si-hsa_circ_000074 组,转染si-nc后将其编为si-nc组,并用qRT-PCR实验检验转染效率,之后进行集落和CCK-8 实验对于si-hsa_circ_000074 组和si-nc组之间的细胞增殖速率进行检验;开展划痕和侵袭实验对于si-hsa_circ_000074 组和si-nc组之间的细胞迁移和侵袭能力进行进行检验.结果 GSE182471 和GSE165884 数据集取交集得出has_circ_0000741 在两个数据集中癌组织组均显著上调;qRT-PCR实验发现hsa_circ_0000741 在正常细胞系中表达量低于癌细胞系,在三阴性细胞系MDA-MB-231 较MCF-7 更为显著;集落和CCK-8 实验显示si-hsa_circ_000074 组的增殖速率明显低于si-nc组;划痕和侵袭实验表明si-hsa_circ_000074 组的迁移和侵袭能力明显弱于si-nc组.结论 Hsa_circ_0000741 在乳腺癌中显著高表达,下调其表达抑制乳腺癌细胞增殖、迁移和侵袭.

Abstract Purpose FDX1 is a key gene regulating cuproptosis, but there is no pan-cancer analysis. We performed a pan-cancer analysis of FDX1 using bioinformatics techniques to derive the effect of FDX1 on the immune mechanisms and prognostic value of cancer patients.Methods We comprehensively investigated the expression profile of FDX1 using the Timer, TCGA, and GTEx databases, we established Cox proportional hazards regression models to evaluate the prognostic value of FDX1. cBioPortal database was used to study the frequency of changes and mutations of FDX1, the ULCAN database for FDX1 phosphorylation, sites, and using GSCA database to investigate the FDX1 DNA methylation in different cancers. The effect of FDX1 on immune mechanisms in various types of cancers was investigated. FDX1-related genes were collected using the gepia database, we performed GO enrichment and KEGG pathway analysis on FDX1 and FDX1-related genes, and single-gene GSEA pathway analysis was performed. We used String database to draw the Protein-Protein Interaction Networks of FDX1.Result FDX1 expression showed a significant downward trend in most tumors and was strongly associated with prognosis in some tumors. We observed elevated phosphorylation levels at the S177 site of KIRC or LUAD and decreased phosphorylation levels at the S159 and S177 sites of LIHC. There is a certain correlation between FDX1 DNA methylation and mRNA expression which related to the prognosis of the tumors. The proportion of immune cells in each tumor was essentially the same except for UVM. In LGG, KIRP and THCA, FDX1 expression was significantly correlated with immune infiltrating cells, it was significantly correlated with the levels of most immune-related genes. The correlation between FDX1 and TMB and MSI may provide a basis for drug use in certain tumors.Conclusion FDX1 can be used as a prognostic marker for some tumors.